Abstract
Background: Bronchial epithelial to mesenchymal transition （EMT）is an important mechanism for the airway remodeling in asthmatics. Mast cell is one of the critical effector cells in pathogenesis of asthma. Although mast cells have been shown to release a plethora of pro-fibrotic factors with the potential to induce EMT, it is not clear whether mast cells also directly have an impact on the bronchial EMT. In this study, we investigated the contribution of human mast cells to EMT in human bronchial epithelial cell line 16-HBE. Methods: Human peripheral blood-derived mast cells were co-cultured with 16-HBE cells. The protein and mRNA expression of E-cadherin and vimentin in 16-HBE cells were analyzed by Western blot and quantitative real-time PCR. A scratch wound assay was performed to evaluate the migratory properties of the 16-HBE cells.Results: Mast cells alone failed to produce significant effects on the epithelial morphology, mobility, and expression of E-cadherin and vimentin. However, mast cells in combination of interleukin (IL)-1β significantly decreased E-cadherin expression but increased vimentin expression in the co-cultured 16-HBE cells, which exhibited a spindle-like appearance with reduced cell junctions and enhanced migration. The down-regulation of E-cadherin expression and up-regulation of vimentin expression were not abrogated by the transforming growth factor (TGF)-β1 neutralizing antibody.Conclusion: Mast cells combined with IL-1β, not mast cells alone, were able to induce EMT in 16-HBE cells through a TGF-β1-independent mechanism. The results of in vitro culture suggest the possibility that mast cells contribute to human bronchial epithelial EMT in the asthmatic airway tissues with high level of IL-1β.
INHIBITORY ACTIVITY OF MITE IgG4 ANTIBODY ON ANTIGEN-INDUCED HISTAMINE RELEASE FROM HUMAN PERIPHERAL BLOOD LEUKOCYTES